Several features of AV conduction are of physiological and clinical significance. The principal delay in conduction of impulses from the atria to the ventricles occurs in the AN and N regions of the AV node. Conduction velocity is actually less in the N region than in the AN region. However, the path length is substantially greater in the AN region than in the N region. Conduction times through the AN and N regions account for the delay between the start of the P wave (the electrical manifestation of atrial excitation) and the QRS complex (the electrical manifestation of ventricular excitation) on an ECG (see the section “
Electrocardiography”).
In terms of function, the delay between atrial and ventricular excitation enables optimal ventricular filling during atrial contraction.
In the N region, slow-response action potentials prevail. The resting potential is approximately −60 mV, the upstroke velocity is low (≈5 V/sec), and the conduction velocity is approximately 0.05m/sec.
Tetrodotoxin, which blocks the fast sodium channels, has virtually no effect on action potentials in this region (or on any other slow-response fibers). Conversely, calcium channel antagonists decrease the amplitude and duration of the action potentials (
Fig.
16.21 ) and depress AV conduction.
bThe shapes of the action potentials in the AN region are intermediate between those in the N region and those in the atria. Similarly, action potentials in the NH region are transitional between those in the N region and those in the bundle of His.
CHAPTER 16 Elements of Cardiac Function
Like other slow-response action potentials, the relative refractory period of cells in the N region extends well beyond the period of complete repolarization; that is, these cells display postrepolarization refractoriness (see
Fig. 16.15 ). As the heart rate increases, the time between successive atrial depolarizations is decreased, and conduction through the AV junction slows. Abnormal prolongation of the AV conduction time is called a first-degree AV block (see the section ”). Most of the prolongation of AV conduction induced by an increase of atrial frequency takes place in the N region of the AV node.
Impulses tend to be blocked in the AV node at stimulation frequencies that are easily conducted in other regions of the heart. If the atria are depolarized at a high repetition rate, only a fraction (e.g., half) of the atrial impulses might be conducted through the AV junction to the ventricles. The conduction pattern in which only a fraction of the atrial impulses are conducted to the ventricles is called a second-degree AV block (see the section ”). This type of block may protect the ventricles from excessive contraction frequencies, wherein the filling time between contractions might be inadequate.
Retrograde conduction can occur through the AV node. However, the conduction time is significantly longer, and the impulse is blocked at lower repetition rates when the impulse is conducted in the retrograde instead of the ante-grade direction. In addition, the AV node is a common site for reentry (see the section “
As in the SA node, the autonomic nervous system regulates AV conduction. Weak vagal activity may simply prolong the AV conduction time. Thus for any given atrial cycle length, the atrium-to-His or atrium-to-ventricle conduction time is prolonged by vagal stimulation. Stronger vagal activity may cause some or all of the impulses arriving from the atria to be blocked in the node. The conduction pattern in which none of the atrial impulses reaches the ventricles is called a third degree, or complete, AV block (see the section ”). The vagally induced delay or absence of conduction through the AV node occurs mainly in the N region. This effect of vagal stimulation reflects the action of acetylcholine to hyperpolarize the membrane of the conducting fibers in the N region (Fig. 16.22 ). The greater the hyperpolarization at the time of arrival of the atrial impulse, the more impaired the AV conduction.